TY - JOUR
T1 - Senescence-related myocardial dysfunction
T2 - keeping a young heart
AU - Ajjan, Ramzi A
AU - Huckstepp, Robert T R
AU - Akbar, Naveed
AU - Bauersachs, Johann
AU - Lok, Jesher Ching Wai
AU - Choppy-Madeleine, Juel
AU - Christopher, Gary
AU - Dalakoti, Mayank
AU - Dawson-Plincke, Emily
AU - Dodds, John
AU - Ellison-Hughes, Georgina M
AU - Emanueli, Costanza
AU - George, Christopher H
AU - Goyal, Anushka
AU - Higginbotham, Victoria
AU - Holzner, Lorenz
AU - Kanamarlapudi, Venkateswarlu
AU - Madeddu, Paolo
AU - Mauro, Claudio
AU - Lewis-McDougall, Fiona
AU - Murray, Andrew J
AU - Damien Genetus, Renita Peter
AU - Short, Emma
AU - Sussman, Mark A
AU - Tavares, Adriana A S
AU - Thompson, Samuel
AU - Wadodkar, Morya
AU - Calimport, Stuart R G
AU - Bentley, Barry L
N1 - Publisher Copyright:
© The Author(s) 2026.
PY - 2026/3/6
Y1 - 2026/3/6
N2 - The ageing heart undergoes progressive and substantial changes. Myocardial cells enter a senescence-associated secretory phenotype (SASP), associated with alterations in extracellular vesicles (EVs) containing microRNAs, creating an inflammatory environment. These molecular changes, combined with mitochondrial dysfunction, induce myocardial cell hypertrophy, multinucleation, and also result in altered responses to autonomic regulation. Alongside the stress of the continuous workload on the heart over a lifetime, there is a reduction in repair mechanisms, which coupled with fibrosis, steatosis, valve stenosis and compromised blood supply, due to atherosclerosis, ultimately lead to organ dysfunction, and myocardial ageing. Created in Biorender. For image description, please refer to the figure legend and surrounding text.
AB - The ageing heart undergoes progressive and substantial changes. Myocardial cells enter a senescence-associated secretory phenotype (SASP), associated with alterations in extracellular vesicles (EVs) containing microRNAs, creating an inflammatory environment. These molecular changes, combined with mitochondrial dysfunction, induce myocardial cell hypertrophy, multinucleation, and also result in altered responses to autonomic regulation. Alongside the stress of the continuous workload on the heart over a lifetime, there is a reduction in repair mechanisms, which coupled with fibrosis, steatosis, valve stenosis and compromised blood supply, due to atherosclerosis, ultimately lead to organ dysfunction, and myocardial ageing. Created in Biorender. For image description, please refer to the figure legend and surrounding text.
U2 - 10.1093/eurheartj/ehag095
DO - 10.1093/eurheartj/ehag095
M3 - Review article (Academic Journal)
C2 - 41790041
SN - 0195-668X
JO - European Heart Journal
JF - European Heart Journal
M1 - ehag095
ER -